As acknowledged by the original investigators, the observed DT4-placebo difference in overall mortality is not statistically significant as judged by the statistical methods utilized in this study.44 Nevertheless, given the mortality trend and the low probability of eventual benefits, a decision was made to discontinue the DT4 arm. In discontinuing the DT4 arm, the study leadership recognized that the findings of the CDP left open the possibility that dextrothyroxine may be efficacious for a limited group of carefully selected myocardial infarction (MI) patients and for persons free of clinical CHD. 44 The net effect of DT4 on serum lipids (the observed fall corrected for the concomitant rise for the placebo group) was a sustained significant fall from baseline levels. The decrease was approximately 12% in serum cholesterol levels and 15-20% in fasting serum triglyceride levels.44 Following the study, it was revealed that the DT4 dispensed in the study contained less than 0.5% of levothyroxine (approximately 30 µg of levothyroxine).44 Interestingly, it was later found that contamination of levothyroxine commercial preparations varied from lot to lot (from 0.5% to 2.3%).45 Also, this "DT4" formulation had other significant thyromimetic effects, leading to TSH suppression that may have become clinically relevant with prolonged use.47 Suboptimal dosing and thyrotoxic effects due to drug contamination may explain why more than 40% of the DT4 patients required a dose reduction.44 1.1.3 DITPA DITPA (3,5-diiodothyropropionic acid) is an analogue of naturally occurring thyroid hormone (T3) that has been specifically designed to improve cardiac performance with a lower potential for tachycardia.22, 40, 46 DITPA binds to the same thyroid hormone receptors α and β as T3 but with less affinity.41 In pre-clinical animal post-infarction models, DITPA improved calcium handling, promoted angiogenesis, and attenuated abnormal left ventricular remodeling.47-53 In a rat model of CHF, DITPA demonstrated increased cardiac output with increases in left ventricular dp/dt, comparable to effects seen with T4, but with significantly less tachycardia. In addition, there were increases in α-myosin heavy chain (MHC) RNA gene expression induced by DITPA treatment.41 When evaluated in combination with captopril, DITPA improved both cardiac output and dp/dt as well as increased the rate of LV relaxation when compared with captopril alone.54 In a rabbit post-infarction model, DITPA decreased left ventricular end diastolic pressure and increased positive and negative dp/dt without changes in heart rate or left ventricular systolic pressure.43 In the same model, use of DITPA prevented abnormal SERCA transport and abnormal contractile function associated with myocardial infarction.42, 44 Recently DITPA was also noted to improve endothelial function following myocardial infarction, an action mediated through nitric oxide.55 The objective of the present study is to evaluate the feasibility of DITPA, a thyroid hormone analogue, as a potential lipid modification agent.